Dexamethasone does not affect vasopressin release in bronchopulmonary dysplasia

Elevated levels of vasopressin (AVP) have been found in premature infants with bronchopulmonary dysplasia (BPD), and may be related to abnormalities of water handling, and to non-pulmonary signs of edema. Dexamethasone treatment improves pulmonary function in infants with BPD, and is frequently associated with a significant increase in diuresis and a decrease in weight gain. To determine whether this diuresis is primarily the result of AVP inhibition (potentially induced by steroid treatment), we measured endogenous AVP levels in nine premature babies with BPD [birth weight 802 +/- 141 (SD) g; gestation 26 +/- 2 weeks, age 26 +/- 17 days], before initiation, and 3 and 7 days after the start of dexamethasone therapy (0.5 mg/kg/day). All study infants required mechanical ventilation, and none was receiving diuretics or cardiac inotropes during the study. Results indicated that premature infants with BPD have functionally unmodified AVP levels after 3 and 7 days of dexamethasone therapy (pre-dexamethasone 5.9 +/- 2.1 ng/l vs post-dexamethasone 7.0 +/- 3.0 and 8.0 +/- 1.9 ng/l at 3 and 7 days, respectively). Pulmonary function improved with oxygenation indexes decreasing (pre-dexamethasone 14 +/- 7 vs post-dexamethasone 9 +/- 7 and 7 +/- 4 at 3 and 7 days, respectively). A concurrent reduction in weight gain occurred (pre-dexamethasone 12 +/- 10 g/kg/day vs post-dexamethasone 7 +/- 3 g/kg/day and 3 +/- 1.5 g/kg/day on days 3 and 7, respectively). These data suggest that the improvement in lung function with dexamethasone treatment for BPD in premature infants does not correlate with a diuresis that results from vasopressin inhibition, and potentially induced by dexamethasone.